Fungi Flashcards

1
Q

What species of candida accounts for 50% of all candida infections?

A

c. albicans

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2
Q

How does oral candida infection occur?

A

usually the result of the outgrowth of an endogenous pop of candida organisms no longer held in check by innate body defenses

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3
Q

What are the three main body defenses that usually help prevent candida from infecting the oral cavity?

A

saliva and normal bacterial flora and t cell mediated immunity

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4
Q

For what kinds of patients is candida especially dangerous (ie. what cell deficiencies)?

A

t-lymphocyte defects or neutropenic pts with disseminated infection have very poor prognosis

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5
Q

What is a fungal infection that is considered an AIDS-defining illness? What are associated problems?

A

candida esophagitis
dysphagia/difficulty swallowing. often consume soft carb-rich diets as a result- bad cycle, since such diets lower the environmental pH, which makes candida happy

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6
Q

What are the morphologic forms of candida?

A

yeast, hypha, pseudohypha

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7
Q

What is candida vulvovaginitis? what species cause this infection? How is it treated

A

“yeast infection”
candida albicans
candida glabrata (higher rates of treatment failure)
fluconazole

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8
Q

What distinguishes C. albicans from other candida species?

A

ability to form germ tubes- nascent hypha from yeast forms

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9
Q

What form(s) of candida is/are most adhesive?

A

germ tube and mature hyphae

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10
Q

How does candida adhere to the oral cavity?

A

host transglutaminase interacts with candida integrin or proline-rich molecules to provide a stable, covalent attachment.

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11
Q

How does C. albicans invade tissue?

A

growing hyphal tip actively penetrates tissue. facilitated by secretion of hydrolytic enzymes

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12
Q

What are the three main layers of the candida cell wall?

A

mannoprotein layer
glucan layer
chitin layer

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13
Q

What is the purpose of the mannan/mannoprotein layer in candida?

A

attachement and permeability barrier

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14
Q

What is the role of the glucan layer in candida?

A

structural integrity of the cell

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15
Q

What is the role of the chitin layer in candida?

A

structural role, esp. at the site of new cell formation

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16
Q

What are polyene antibiotics? What are the two relevant drugs? How does it work?

A

example: amphotericin B and nystatin

this binds to ergosterol in the plasma membrane and increases its permeability.

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17
Q

What are special considerations with the use of amphotericin B>

A

amphotericin B cannot be orally administered because its not water soluble.

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18
Q

Are polyene antibiotics -cidal or -static drugs? Any special considerations/concerns?

A

cidal

yes! very low therapeutic window

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19
Q

What are the azole derivatives (imidazoles and triazoles)? (examples) How do they work?

A

miconazole and fluconazole
perturb membrane stucture and function by inhibition of a cytochrome P450 analog which participates in the synthesis of membrane components

20
Q

What is miconazole? What class and how administered?

A
azole derivative (fungal P450 inhibitor and membrane synthesis disruptor)
topical application
21
Q

What is fluconazole? What class and how administered?

A

triazole derivative
P450 analog inhibitor- membrane synthesis disruptor
systemic admin

22
Q

Are azole derivatives -cidal or -static agents?

A

static

23
Q

Echinocandins. How do they work? Example?

A

caspofungin

target beta-glucans by inhibiting glucan synthesis

24
Q

Are echinocandins -cidal or -static agents?

A

cidal

25
Q

Flucytosine: how does it work? How administered? special considerations?

A

nucleic acid analog that inhibits DNA synthesis. good oral absorption
relatively low toxicity but must be used in conjunction with other drugs because resistance develops easily

26
Q

What is cryptococcus neoformans? Who is susceptible? Morphology? reservoir?

A

most rapidly emerging fungal pathogen for AIDS pts
yeast form only
pigeon droppings and eucalyptus leaves

27
Q

What is the main virulence factor associated with cryptococcus neoformans? What is the main therapeutic challenge?

A
  • polysacchride capsule

- reistant to echinocandins

28
Q

Aspergillus: who is susceptible? Where is it acquired? What happens during infection

A
  • those with severe breakdown in cell-mediated defenses
  • acquired by inhalation of ubiquitous spores
  • grow as filamentous form at the site of infection to form a fungal ball or aspergilloma
  • secrete hydrolytic proteases
29
Q

How do you treat aspergillus infection?

A

amphotericin B

30
Q

What is dermatophytosis? What layer of the skin is infected? What are the two main genera?

A

fungal infection of keratinized tissue
stratum corneum is infected
trichophyton and microsporum

31
Q

What is an effective drug against the dermatophytes?

A

allylamines, like terbinafine/lamisil

32
Q

How do allylamines work?

A

inhibit squalene epoxidase, which is needed for ergosterol formation. leads to membrane disruption and cell death.

33
Q

What are two licensed allylamines?

A

lamisil/terbinafine and naftifine

34
Q

How is terbinafine administered? How is naftifine administered?

A

terbinafine is available both orally and topically

naftifine is only topical

35
Q

What are the 5 traits common to systemic mycoses caused by environmentally acquired fungi?

A
  1. dimorphism- grow in yeast form at 37C (as mycelium at 25C)
  2. route of infection- inhalation of spores
  3. disseminated infection, esp. in immunocompromised
  4. geographic predilection
  5. immunologic response, usually granulomatous inflammation
36
Q

What are some symptoms of systemic mycoses?

A

often asymptomatic
may present with severe pulmonary disease and weight loss
you must differentiate btw systemic mycoses and TB

37
Q

Where is histoplasma capsulatum common? Where is it found in the environment?

A

ohio, mississippi and missouri river valleys
found in bird and bat feces
acute and chronic pulmonary infections

38
Q

Pathology of histoplasma capsulatum

A

reporduces inside macrophages
usually asymptomatic
some people get headaces, fevers, chills, cough, chest pain.

39
Q

Coccidioides immitis: where is it common geographically?

A

dsserts of northern mexico and SW US.

40
Q

Coccidioides immitis- typical presentations? severe presentations

A

often asymptomatic
sometimes flu symptoms- fever, dry cough, eosinophili, etc.
some get bone infection and meningitis (less than 1%)

41
Q

Blastomyces dermatitidis. where is it found geographically and environmentally?

A

soil of states east of the mississippi

42
Q

What are symptoms of bastomyces dermatitidis?

A

rarely asymptomatic
usually pleuritic chest pain, fever, chills, productive cough
severe cases involve weight loss, night sweats, skin ulcers, potential death. TREAT AGGRESSIVELY.

43
Q

Paracoccidioides brasiliensis: morphology. where is it from?

A

pilots wheel- multiple buds off a single parent cell

endemic to brazil and latin america

44
Q

What is the epi of paracoccidioides brasiliensis? What are the most common sites of infection?

A
  • WAY more men than women (female hormones prevent infection?)
  • mouth and nose
45
Q

What are the four systemic mycoses?

A

coccidioides immitis, histoplasma capsulatum, blastomyces dermatitidis, and para coccidioides brasiliensis